From these studies, the investigators have evidence to suggest that stress-related events can influence allergic inflammation and, presumably, that these peripheral responses are regulated by central nervous system (CNS) events. Although stress-related events can modulate inflammatory processes, the mechanisms and CNS-site of this activity are poorly understood. It is proposed that areas of the brain are activated by stress and that these areas of activation may represent sites in the CNS that integrate information concerning the internal state of the body and signal the generation of modulating factors in the enhancement or inhibition of the allergic airway inflammation. To visualize these potential sites of CNS activation in asthma, it is possible to use neuroimaging techniques, such as positron emission tomography (PET) or functional magnetic resonance imaging (fMRI). The investigators have completed two prior studies that used fMRI to evaluate the central mechanisms associated with allergic inflammation, and in both studies, the anterior insula was identified as a region activated by asthma-related emotional cues that predicted the subsequent development of airway inflammation (e.g. Rosenkranz, M et al (2005) Proceedings of the National Academy of Science 102, 13319-13324.). In addition, the investigators have completed a study using PET to evaluate the neural mechanisms through which stress along contributes to asthma-related inflammation in individuals with high and low levels of chronic stress. This study corroborated our findings using fMRI, showing involvement of the insula, and also revealed new mechanisms involving IL-1β/IL-17 as a potential pathway linking through which stress-reactivity primes airway inflammation.